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CCAAT/enhancer binding protein beta deficiency provides cerebral protection following excitotoxic injury

AuthorsCortés-Canteli, Marta ; Luna Medina, Rosario de ; Sanz-SanCristóbal, Marina ; Álvarez Barrientos, Alberto; Santos, Ángel; Pérez Castillo, Ana
Issue Date15-Apr-2008
PublisherCompany of Biologists
CitationJournal of Cell Science 121(8): 1224-1234 (2008)
AbstractThe CCAAT/enhancer-binding protein beta (C/EBPbeta, also known as CEBPB) was first identified as a regulator of differentiation and inflammatory processes in adipose tissue and liver. Although C/EBPbeta was initially implicated in synaptic plasticity, its function in the brain remains largely unknown. We have previously shown that C/EBPbeta regulates the expression of genes involved in inflammatory processes and brain injury. Here, we have demonstrated that the expression of C/EBPbeta is notably increased in the hippocampus in a murine model of excitotoxicity. Mice lacking C/EBPbeta showed a reduced inflammatory response after kainic acid injection, and exhibited a dramatic reduction in pyramidal cell loss in the CA1 and CA3 subfields of the hippocampus. These data reveal an essential function for C/EBPbeta in the pathways leading to excitotoxicity-mediated damage and suggest that inhibitors of this transcription factor should be evaluated as possible neuroprotective therapeutic agents.
Description11 pages, 7 figures.-- Supplementary material available online at http://jcs.biologists.org/cgi/content/full/121/8/1224/DC1
Publisher version (URL)http://dx.doi.org/10.1242/jcs.025031
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